Introduction to decadron (dexamethasone)
Decadron is a brand name for dexamethasone, a potent synthetic glucocorticoid medication that belongs to the corticosteroid class of drugs. Dexamethasone is widely recognized as one of the most powerful anti-inflammatory and immunosuppressive agents in clinical use, possessing approximately 25 times the anti-inflammatory potency of the naturally occurring hormone cortisol and 5 to 6 times that of prednisone. Since its introduction into medical practice, Decadron has become an indispensable therapeutic tool across virtually every medical specialty, from rheumatology and pulmonology to neurology and oncology. Patients seeking reliable access to this important medication can find it through a Happy Family Store, which offers competitive pricing on a comprehensive range of pharmaceutical products.
Dexamethasone exerts its effects by binding to the glucocorticoid receptor, a nuclear receptor that functions as a transcription factor to regulate gene expression. This interaction leads to widespread changes in protein synthesis that ultimately suppress inflammation, modulate immune responses, and alter metabolism throughout the body. The medication is available in numerous formulations including oral tablets, oral solution, injectable solutions for intravenous and intramuscular use, topical preparations, ophthalmic drops and ointments, and aerosol inhalers, making it adaptable to a wide variety of clinical situations.
The unique pharmacological properties of dexamethasone include its long duration of action, its minimal mineralocorticoid activity compared to other corticosteroids, and its excellent penetration into the central nervous system. These characteristics make Decadron particularly useful for conditions requiring sustained anti-inflammatory effects, situations where fluid retention is undesirable, and disorders affecting the brain and spinal cord such as cerebral edema and multiple sclerosis.
Medical uses and indications
Decadron is approved for use in a broad spectrum of medical conditions. In endocrinology, dexamethasone is used for diagnostic purposes in the dexamethasone suppression test, which evaluates adrenal gland function and helps diagnose conditions such as Cushing’s syndrome. The medication can also be used as replacement therapy for patients with primary or secondary adrenal insufficiency, though it is not typically the first choice for this indication due to its long duration of action and lack of mineralocorticoid activity.
In rheumatology and orthopedics, dexamethasone injections are frequently administered directly into inflamed joints, bursae, and tendon sheaths for the treatment of osteoarthritis, rheumatoid arthritis, gout, bursitis, tendinitis, and epicondylitis (tennis elbow). Intra-articular and periarticular injections deliver a high concentration of the medication precisely to the site of inflammation, providing rapid and sustained relief that can last for weeks to months with minimal systemic exposure.
Respiratory conditions including severe asthma, chronic obstructive pulmonary disease (COPD), and croup in children are often treated with dexamethasone. In acute asthma exacerbations, early administration of oral or intravenous dexamethasone can reduce airway inflammation, improve lung function, and decrease the need for hospitalization. For croup, a single dose of oral dexamethasone has been shown to reduce symptom severity and shorten the duration of illness.
Neurological applications of Decadron are particularly important. Cerebral edema associated with brain tumors, neurosurgery, or traumatic brain injury is a major indication for high-dose dexamethasone, as the medication’s excellent blood-brain barrier penetration allows it to effectively reduce intracranial pressure and prevent potentially fatal brain herniation. Dexamethasone is also used in the acute treatment of multiple sclerosis relapses, where it can accelerate recovery from neurologic deficits by reducing inflammation and demyelination within the central nervous system.
In oncology, dexamethasone serves multiple roles. It is used as a component of antiemetic regimens to prevent chemotherapy-induced nausea and vomiting, particularly in combination with serotonin 5-HT3 receptor antagonists and neurokinin-1 receptor antagonists. Decadron is also used to treat tumor-related edema and inflammation, to manage pain from bone metastases, and as a chemotherapeutic agent itself in the treatment of certain hematologic malignancies including multiple myeloma, lymphoma, and leukemia.
Ophthalmic conditions treated with topical dexamethasone include non-infectious uveitis, iritis, choroiditis, allergic conjunctivitis, and inflammatory conditions of the eyelids and cornea. The anti-inflammatory effects help preserve vision by reducing swelling and preventing scar formation in delicate ocular tissues. However, ophthalmic corticosteroids require careful monitoring due to the risks of increased intraocular pressure and cataract formation.
Dermatological uses of dexamethasone include the treatment of severe inflammatory skin conditions such as pemphigus, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), and severe psoriasis. Topical and systemic dexamethasone can rapidly control disease activity in these conditions, though long-term use is limited by the potential for significant side effects.
Gastrointestinal conditions including ulcerative colitis and Crohn’s disease may benefit from short-term dexamethasone therapy during acute exacerbations. The medication reduces intestinal inflammation, controls diarrhea, and promotes mucosal healing. However, due to the risks associated with prolonged corticosteroid use, dexamethasone is typically reserved for acute management rather than maintenance therapy in inflammatory bowel disease.
Dosage forms and strengths
Decadron is available in multiple formulations with widely varying strengths appropriate for different indications. Oral dexamethasone tablets are typically available in 0.5 mg, 0.75 mg, 1 mg, 1.5 mg, 2 mg, 4 mg, and 6 mg strengths. The 4 mg tablet is one of the most commonly used strengths for systemic therapy. The dosing range for oral dexamethasone varies enormously depending on the condition being treated, from physiologic replacement doses of 0.5 mg to 1 mg daily up to pharmacologic doses of 10 mg to 100 mg daily for severe inflammatory conditions or cerebral edema.
Oral dexamethasone solution is available in concentrations of 0.5 mg per 5 mL and 1 mg per mL, providing dose flexibility for pediatric patients and adults who cannot swallow tablets. The solution is particularly useful for patients requiring very low doses or precise dose titration.
Injectable dexamethasone is available as dexamethasone sodium phosphate, a water-soluble salt that can be administered intravenously, intramuscularly, intra-articularly, intralesionally, or by soft tissue injection. The injectable formulation is typically available in concentrations of 4 mg/mL, 10 mg/mL, and 20 mg/mL, with dosing adjusted based on the route of administration and the condition being treated.
Ophthalmic dexamethasone preparations include 0.1% ophthalmic solution (eyedrops) and 0.05% ophthalmic ointment, typically dosed 3 to 6 times daily initially with tapering as inflammation resolves. Topical dexamethasone creams and lotions are available in 0.1% concentration for dermatological use. Dexamethasone elixir is available for oral administration in a flavored alcohol-based vehicle.
Mechanism of action
The therapeutic effects of dexamethasone are mediated through its interaction with the glucocorticoid receptor, a member of the nuclear receptor superfamily of transcription factors. When dexamethasone diffuses across the cell membrane and binds to the glucocorticoid receptor in the cytoplasm, the receptor undergoes a conformational change that releases it from a complex of heat shock proteins and other chaperone molecules that keep it in an inactive state.
The activated receptor-ligand complex then translocates into the cell nucleus, where it binds to specific DNA sequences known as glucocorticoid response elements (GREs) located in the promoter regions of target genes. Binding to GREs can either increase (transactivation) or decrease (transrepression) the transcription of nearby genes, leading to altered production of the corresponding proteins. Transactivation is responsible for many of the metabolic effects of corticosteroids, including increased gluconeogenesis and protein catabolism, while transrepression is primarily responsible for the anti-inflammatory and immunosuppressive effects.
Dexamethasone suppresses the inflammatory response at multiple levels. It increases the production of anti-inflammatory proteins such as lipocortin-1 (which inhibits phospholipase A2 and thereby reduces prostaglandin and leukotriene synthesis), interleukin-10 (an anti-inflammatory cytokine), and I-kappa-B-alpha (which inhibits the pro-inflammatory transcription factor NF-kappa-B). Simultaneously, it decreases the production of pro-inflammatory mediators including numerous cytokines (interleukin-1, interleukin-2, interleukin-6, tumor necrosis factor-alpha), chemokines, adhesion molecules, and enzymes such as cyclooxygenase-2 and inducible nitric oxide synthase.
The immunosuppressive effects of dexamethasone result from its ability to inhibit the proliferation, differentiation, and function of various immune cells. It suppresses T lymphocyte activation and cytokine production, inhibits B lymphocyte antibody production, reduces the antigen-presenting capacity of macrophages and dendritic cells, and decreases eosinophil and basophil survival. These effects are beneficial in autoimmune and allergic conditions and increase susceptibility to infections.
The minimal mineralocorticoid activity of dexamethasone is a significant clinical advantage. Unlike cortisol, hydrocortisone, and prednisolone, dexamethasone has virtually no effect on sodium retention, potassium excretion, or water balance at therapeutic doses. This makes Decadron the preferred corticosteroid for patients with hypertension, congestive heart failure, or other conditions where fluid retention would be particularly problematic.
Side effects and adverse reactions
While Decadron is highly effective for many conditions, its use is associated with a wide spectrum of potential adverse effects, particularly when high doses are used or when treatment is prolonged. The side effect profile of dexamethasone is qualitatively similar to that of other systemic glucocorticoids, though the incidence and severity of specific effects may differ due to its potency and long duration of action.
Metabolic and endocrine effects are among the most common concerns. Dexamethasone can cause hyperglycemia and worsen glycemic control in diabetic patients, and even patients without pre-existing diabetes may develop steroid-induced hyperglycemia or, rarely, steroid-induced diabetes mellitus. Increased appetite and weight gain are frequently reported, and chronic use leads to the characteristic cushingoid habitus including moon face, buffalo hump, central obesity, and thinning of the extremities.
Musculoskeletal side effects are significant, particularly with long-term use. Dexamethasone inhibits bone formation and increases bone resorption, leading to decreased bone mineral density and an increased risk of osteoporotic fractures. Avascular necrosis (osteonecrosis) of the femoral head and other bones is a particularly serious complication that can cause severe pain and disability, often requiring joint replacement surgery. Myopathy with proximal muscle weakness, particularly affecting the thighs and shoulders, may also develop.
Gastrointestinal effects include an increased risk of peptic ulcer disease, gastritis, pancreatitis, and esophageal candidiasis. Dexamethasone can mask the symptoms of gastrointestinal perforation and peritonitis, potentially delaying diagnosis of these life-threatening conditions. Patients with a history of peptic ulcer disease should receive appropriate gastroprotective therapy when corticosteroids are necessary.
Cardiovascular effects include hypertension, although this is less common with dexamethasone than with corticosteroids having greater mineralocorticoid activity. An increased risk of thromboembolic events, including deep vein thrombosis and pulmonary embolism, has been associated with corticosteroid use. Dyslipidemia and accelerated atherosclerosis are additional cardiovascular concerns with long-term therapy.
Neuropsychiatric effects are common and can range from mild to severe. Euphoria, insomnia, anxiety, and irritability are frequently reported, particularly in the early stages of treatment. More serious neuropsychiatric effects including depression, mania, psychosis, and delirium can occur, especially with high doses. Patients with a personal or family history of psychiatric illness may be at increased risk. Corticosteroid-induced psychiatric disturbances typically resolve with dose reduction or discontinuation.
Dermatological effects include skin thinning, easy bruising, striae (stretch marks), impaired wound healing, acne, and increased susceptibility to skin infections. Topical or systemic corticosteroids can also cause perioral dermatitis and exacerbation of acne rosacea. Ophthalmic effects include the development of posterior subcapsular cataracts and elevation of intraocular pressure (glaucoma), which can occur even with topical ophthalmic use.
Immunosuppression is a major concern with systemic dexamethasone therapy. The medication increases susceptibility to bacterial, viral, fungal, and parasitic infections and can reactivate latent infections including tuberculosis, hepatitis B, herpes simplex, and varicella-zoster virus (shingles). Patients receiving immunosuppressive doses should avoid exposure to infections and receive appropriate vaccinations before initiating therapy when possible.
Drug interactions
Dexamethasone interacts with numerous medications through both pharmacokinetic and pharmacodynamic mechanisms. Nonsteroidal anti-inflammatory drugs (NSAIDs) including ibuprofen, naproxen, and diclofenac, when combined with dexamethasone, increase the risk of gastrointestinal ulceration, bleeding, and perforation. Patients requiring both medications should be monitored closely and considered for gastroprotective therapy.
Anticoagulants such as warfarin may have altered effects when combined with dexamethasone. Corticosteroids can both potentiate and inhibit the anticoagulant effect of warfarin, necessitating more frequent monitoring of the international normalized ratio (INR). Insulin and oral hypoglycemic agents may require dose adjustment when dexamethasone therapy is initiated or discontinued due to the medication’s hyperglycemic effects.
Dexamethasone is metabolized by the CYP3A4 enzyme system and can both induce and be affected by inhibitors and inducers of this enzyme. CYP3A4 inducers such as rifampin, phenytoin, carbamazepine, phenobarbital, and St. John’s wort can increase the clearance of dexamethasone and reduce its effectiveness, potentially requiring dose increases. Conversely, CYP3A4 inhibitors such as ketoconazole, itraconazole, certain protease inhibitors, and grapefruit juice can decrease dexamethasone clearance and increase the risk of toxicity.
Dexamethasone itself is a moderate inducer of CYP3A4, meaning it can increase the metabolism of other drugs that are substrates of this enzyme, potentially reducing their efficacy. This is particularly important for medications with narrow therapeutic indices such as cyclosporine, tacrolimus, and certain anticancer agents. Patients taking these medications may require dose adjustments when dexamethasone therapy is initiated or discontinued.
Contraindications and precautions
Systemic fungal infections are an absolute contraindication to the use of dexamethasone, as the immunosuppressive effects of the medication can allow the infection to disseminate and become life-threatening. However, dexamethasone may be used in patients with fungal infections who are receiving appropriate antifungal therapy, if the benefit of corticosteroid treatment outweighs the risk.
Patients with known hypersensitivity to dexamethasone or any component of the formulation should not receive the medication. Live or live attenuated vaccines should not be administered to patients receiving immunosuppressive doses of corticosteroids, as the immune response may be insufficient to provide protection and there is a risk of vaccine-induced infection. Inactivated vaccines may also be less effective in immunocompromised patients and should ideally be administered before corticosteroid therapy is initiated.
Special caution is required in patients with congestive heart failure, hypertension, or renal impairment, as dexamethasone, despite its minimal mineralocorticoid activity, can still cause fluid retention at high doses. Patients with diabetes should be counseled about the potential for hyperglycemia and instructed to monitor their blood glucose levels more frequently during treatment.
Impact on bone health and osteoporosis prevention
One of the most significant concerns with dexamethasone therapy is its impact on bone metabolism, which can lead to decreased bone mineral density and increased fracture risk. Dexamethasone affects bone through multiple mechanisms, including direct inhibition of osteoblast activity, promotion of osteoclast-mediated bone resorption, suppression of intestinal calcium absorption, and inhibition of gonadotropin secretion leading to hypogonadism. These effects are dose-dependent and most pronounced with long-term therapy, though even short courses of high-dose dexamethasone can cause measurable bone loss.
The risk of corticosteroid-induced osteoporosis is particularly relevant for patients who require multiple or prolonged courses of dexamethasone. Baseline bone mineral density assessment should be considered for patients expected to receive corticosteroid therapy for more than three months. Preventive measures include ensuring adequate calcium (1000 to 1200 mg daily) and vitamin D (600 to 800 IU daily) intake through diet or supplementation. For patients at high risk of fracture, including those with osteopenia, prior fragility fractures, or other risk factors for osteoporosis, bisphosphonate therapy should be considered as first-line prevention.
Regular monitoring with dual-energy X-ray absorptiometry scans every one to two years is recommended for patients on long-term corticosteroid therapy to assess bone density changes and guide treatment decisions. Drug holidays from bisphosphonate therapy may be considered after three to five years in patients who have achieved stable bone density, though corticosteroid-treated patients often require ongoing therapy due to continued bone loss from the underlying treatment.
Use in special populations
Pregnancy: Dexamethasone is classified as FDA Pregnancy Category C. Animal studies have shown an increased risk of cleft palate, intrauterine growth restriction, and other developmental abnormalities with corticosteroid exposure during pregnancy. However, maternal corticosteroid therapy may be necessary for conditions such as autoimmune disease or asthma that, if uncontrolled, pose risks to both mother and fetus. The lowest effective dose should be used for the shortest possible duration.
Breastfeeding: Dexamethasone is excreted in breast milk at concentrations that may be clinically significant, particularly with high maternal doses. The medication may suppress growth and interfere with endogenous corticosteroid production in nursing infants. Breastfeeding should be undertaken with caution in women receiving dexamethasone, and the timing of doses relative to nursing sessions should be optimized to minimize infant exposure.
Pediatric use: Growth suppression is a particular concern with long-term corticosteroid use in children. Growth should be monitored regularly, and the smallest effective dose should be used for the shortest possible duration. Dexamethasone is used in neonates with bronchopulmonary dysplasia and in children with croup, asthma exacerbations, and certain cancers.
Clinical applications in oncology
Decadron plays a multifaceted role in oncology that extends well beyond its antiemetic properties. In multiple myeloma, dexamethasone is a foundation of treatment, used in combination with immunomodulatory drugs such as lenalidomide and pomalidomide, proteasome inhibitors such as bortezomib, and monoclonal antibodies such as daratumumab. The addition of dexamethasone to these regimens improves response rates and survival outcomes, likely through direct cytotoxic effects on myeloma cells, modulation of the tumor microenvironment, and reduction of paraneoplastic symptoms.
In acute lymphoblastic leukemia, dexamethasone is included in virtually all treatment protocols, where it is preferred over prednisone due to its superior penetration into the central nervous system and its potent pro-apoptotic effects on lymphoblasts. The choice between dexamethasone and prednisone in ALL protocols has been studied in randomized trials, with dexamethasone-based regimens showing improved central nervous system relapse prevention and increased toxicity, particularly infectious complications and avascular necrosis.
For the management of brain tumors and cerebral metastases, dexamethasone is the corticosteroid of choice due to its excellent central nervous system penetration and minimal mineralocorticoid activity. High-dose dexamethasone, typically starting at 10 mg to 100 mg daily, rapidly reduces peritumoral edema and lowers intracranial pressure, providing symptomatic relief from headache, nausea, and neurologic deficits. This effect is often dramatic, with improvement occurring within 24 to 48 hours of initiating therapy.
As an antiemetic, dexamethasone is included in virtually all guidelines for the prevention of chemotherapy-induced nausea and vomiting. It enhances the efficacy of serotonin 5-HT3 receptor antagonists and neurokinin-1 receptor antagonists through mechanisms that may include suppression of prostaglandin synthesis, reduction of serotonin release from the gastrointestinal tract, and modulation of neurotransmitter signaling in the vomiting center. The standard dose for antiemetic prophylaxis ranges from 8 mg to 20 mg, administered intravenously before chemotherapy and continued orally for several days following treatment.
Endocrine and diagnostic applications
The dexamethasone suppression test is a critical diagnostic tool in endocrinology for the evaluation of hypercortisolism (Cushing’s syndrome). The test is based on the principle that exogenous dexamethasone suppresses adrenocorticotropic hormone (ACTH) secretion in normal individuals but not in patients with Cushing’s disease or ectopic ACTH production. The overnight 1 mg dexamethasone suppression test is the most commonly used screening test, with a serum cortisol level measured at 8 AM following administration of 1 mg of dexamethasone at 11 PM the previous night. A suppressed cortisol level less than 1.8 mcg/dL effectively excludes Cushing’s syndrome in most patients.
The high-dose dexamethasone suppression test, using 8 mg of dexamethasone, helps differentiate between Cushing’s disease (pituitary ACTH-secreting adenoma) and ectopic ACTH secretion. In Cushing’s disease, the pituitary adenoma typically retains some sensitivity to glucocorticoid negative feedback, resulting in suppression of ACTH and cortisol levels following high-dose dexamethasone. In ectopic ACTH secretion, tumors are generally resistant to glucocorticoid feedback, and cortisol levels do not suppress.
In congenital adrenal hyperplasia, dexamethasone may be used for prenatal treatment to prevent virilization of female fetuses affected by 21-hydroxylase deficiency. Treatment must be initiated very early in pregnancy, before the development of the external genitalia, and requires invasive prenatal diagnostic testing to confirm the diagnosis. This use remains controversial due to concerns about potential long-term effects on the child and the need to treat many fetuses who will ultimately be unaffected.
Infectious disease applications
Dexamethasone has an important role for certain infectious diseases, where its anti-inflammatory effects can reduce morbidity and mortality by dampening harmful host inflammatory responses. In bacterial meningitis, particularly in adults with pneumococcal meningitis, dexamethasone given before or concurrently with the first dose of antibiotics reduces the risk of death and neurologic sequelae. The benefit is attributed to reduction of inflammation-mediated brain injury that occurs as bacteria are killed and release pro-inflammatory cell wall components.
In tuberculous meningitis, dexamethasone therapy has been shown to reduce mortality and improve neurologic outcomes, though the evidence is less conclusive than for bacterial meningitis. The recommended regimen is 8 mg to 16 mg daily tapered over 6 to 8 weeks. The anti-inflammatory effects of dexamethasone help reduce cerebral edema, prevent vasculitis, and control the intense inflammatory reaction that characterizes tuberculous meningitis.
In severe COVID-19, dexamethasone gained international attention following the publication of the RECOVERY trial, which demonstrated that 6 mg of dexamethasone daily for up to 10 days reduced 28-day mortality in hospitalized patients requiring oxygen or mechanical ventilation. This finding established dexamethasone as a standard of care for severe COVID-19 and highlighted the importance of timing in corticosteroid therapy, with benefit confined to patients with significant respiratory compromise and potential harm in patients with milder disease.
Ophthalmic applications
In ophthalmology, dexamethasone is used in various formulations for the treatment of inflammatory conditions of the eye and ocular adnexa. Dexamethasone ophthalmic solution is commonly used for postoperative inflammation following cataract surgery, reducing pain, photophobia, and the risk of cystoid macular edema. The typical regimen involves frequent dosing initially, tapered over several weeks as inflammation resolves. Prolonged use requires monitoring for increased intraocular pressure and cataract formation.
For uveitis, particularly non-infectious uveitis affecting the anterior and intermediate uveal tract, dexamethasone implants provide sustained release of medication directly into the vitreous cavity, achieving high local concentrations with minimal systemic exposure. These implants can provide control of inflammation for up to six months and reduce the need for systemic immunosuppressive therapy. The dexamethasone intravitreal implant is also approved for the treatment of diabetic macular edema and retinal vein occlusion.
Dexamethasone ophthalmic ointment provides prolonged contact time with the ocular surface and is particularly useful for nighttime use or for patients who have difficulty administering eye drops. The ointment formulation is also preferred for the treatment of blepharitis and other eyelid conditions where prolonged drug contact with the eyelid margin is beneficial.
Dermatological applications
In dermatology, topical dexamethasone is used for the treatment of corticosteroid-responsive dermatoses including eczema, psoriasis, contact dermatitis, and seborrheic dermatitis. While dexamethasone is a potent corticosteroid, its topical use is limited by the availability of more potent and specifically formulated topical corticosteroids such as clobetasol propionate and halobetasol propionate. However, dexamethasone remains useful for certain indications, particularly when a fluorinated corticosteroid is desired.
Intralesional dexamethasone injection is used for the treatment of keloids, hypertrophic scars, and certain inflammatory skin conditions such as alopecia areata and discoid lupus erythematosus. The injection delivers a high concentration of corticosteroid directly to the lesion, providing potent anti-inflammatory effects with minimal systemic absorption. Repeated injections at 4 to 6 week intervals are typically required for optimal results.
Anesthetic and perioperative applications
In anesthesiology, dexamethasone is widely used as a component of multimodal analgesia and for the prevention of postoperative nausea and vomiting. A single dose of 4 mg to 8 mg of intravenous dexamethasone at the time of anesthesia induction reduces the incidence of postoperative nausea and vomiting by approximately 30% to 50% and has opioid-sparing effects that reduce postoperative pain. These effects, combined with the low cost and favorable safety profile of single-dose dexamethasone, have made it a standard component of enhanced recovery after surgery protocols.
Dexamethasone is also used as an adjunct to regional anesthesia, prolonging the duration of peripheral nerve blocks when added to local anesthetic solutions. The mechanism appears to involve both local effects on nerve conduction and systemic anti-inflammatory effects that modulate nociceptive signaling. The addition of 4 mg to 8 mg of dexamethasone to bupivacaine or ropivacaine for brachial plexus, femoral, or sciatic nerve blocks can extend analgesia by 6 to 12 hours without significant adverse effects.
Withdrawal and tapering
Abrupt discontinuation of dexamethasone after prolonged use can lead to acute adrenal insufficiency, a potentially life-threatening condition resulting from suppression of the hypothalamic-pituitary-adrenal (HPA) axis. The degree and duration of HPA axis suppression depend on the dose and length of treatment, with higher doses and longer courses causing greater suppression. The recovery of normal adrenal function can take weeks, months, or even years after discontinuation of corticosteroid therapy.
Gradual tapering of dexamethasone is essential to allow recovery of the HPA axis and to prevent the manifestation of adrenal insufficiency. The tapering schedule must be individualized based on the dose, duration of treatment, and the patient’s underlying condition. Patients who have been on corticosteroid therapy should be considered adrenally insufficient during periods of stress such as surgery or severe illness for up to one year after discontinuation and may require stress dose corticosteroid coverage.